Cluster headache pathophysiology: Difference between revisions
No edit summary |
|||
| Line 9: | Line 9: | ||
Cluster headaches are classified as [[vascular headache]]s. The intense pain is caused by the [[dilation]] of blood vessels which creates pressure on the [[trigeminal nerve]]. While this process is the immediate cause of the pain, the [[etiology]] (underlying cause or causes) is not fully understood. | Cluster headaches are classified as [[vascular headache]]s. The intense pain is caused by the [[dilation]] of blood vessels which creates pressure on the [[trigeminal nerve]]. While this process is the immediate cause of the pain, the [[etiology]] (underlying cause or causes) is not fully understood. | ||
<div align="left"> | <div align="left"></div> | ||
</div> | |||
===Hypothalamus=== | ===Hypothalamus=== | ||
| Line 20: | Line 15: | ||
The hypothalamus is responsive to light—[[Circadian rhythm|daylength and photoperiod]]; [[olfactory]] stimuli, including [[pheromone]]s; [[steroid]]s, including [[sex steroids]] and [[corticosteroid]]s; neurally transmitted information arising in particular from the [[heart]], the [[stomach]], and the [[reproductive system]]; [[autonomic]] inputs; [[blood]]-borne stimuli, including [[leptin]], [[ghrelin]], [[angiotensin]], [[insulin]], [[pituitary]] [[hormone]]s, [[cytokine]]s, [[blood plasma]] concentrations of [[glucose]] and [[Osmole (unit)|osmolarity]]; [[Stress (medicine)|stress]]; ''etc''. These particular sensitivities may underlay the causes, triggers, and methods of treatment of cluster headaches. | The hypothalamus is responsive to light—[[Circadian rhythm|daylength and photoperiod]]; [[olfactory]] stimuli, including [[pheromone]]s; [[steroid]]s, including [[sex steroids]] and [[corticosteroid]]s; neurally transmitted information arising in particular from the [[heart]], the [[stomach]], and the [[reproductive system]]; [[autonomic]] inputs; [[blood]]-borne stimuli, including [[leptin]], [[ghrelin]], [[angiotensin]], [[insulin]], [[pituitary]] [[hormone]]s, [[cytokine]]s, [[blood plasma]] concentrations of [[glucose]] and [[Osmole (unit)|osmolarity]]; [[Stress (medicine)|stress]]; ''etc''. These particular sensitivities may underlay the causes, triggers, and methods of treatment of cluster headaches. | ||
The above [[Positron emission tomography]] pictures indicate the brain areas which are activated during pain only, compared to the pain free periods. These pictures show [[brain]] areas which are always active during pain in the yellow/orange color (called "pain matrix"). The area in the center (in all three views) is specifically activated during cluster headache only. The bottom row [[Voxel-based morphometry]] (VBM) pictures show [[structural]] brain differences between cluster headache patients and people without headaches. Only one area is different: This area is identical with the area of CH specific pain. This area is the [[hypothalamus]].<ref>May et al.: PET and MRA findings in cluster headache and MRA in experimental pain ''Neurology'' 2000;'''55''':1328-1335, PMID 11087776.</ref><ref> Dasilva AF, Goadsby PJ, Borsook D: Cluster headache: a review of neuroimaging findings. ''Curr Pain Headache Rep.'' 2007;'''11(2)''':131-6. PMID 17367592.</ref> | The above [[Positron emission tomography]] pictures indicate the brain areas which are activated during pain only, compared to the pain free periods. These pictures show [[brain]] areas which are always active during pain in the yellow/orange color (called "pain matrix"). The area in the center (in all three views) is specifically activated during cluster headache only. The bottom row [[Voxel-based morphometry]] (VBM) pictures show [[structural]] brain differences between cluster headache patients and people without headaches. Only one area is different: This area is identical with the area of CH specific pain. This area is the [[hypothalamus]].<ref>May et al.: PET and MRA findings in cluster headache and MRA in experimental pain ''Neurology'' 2000;'''55''':1328-1335, PMID 11087776.</ref><ref> Dasilva AF, Goadsby PJ, Borsook D: Cluster headache: a review of neuroimaging findings. ''Curr Pain Headache Rep.'' 2007;'''11(2)''':131-6. PMID 17367592.</ref> | ||
===Genetics=== | ===Genetics=== | ||
There is a [[genetics|genetic]] component to cluster headaches, although no single [[gene]] has been identified as the cause. First-degree relatives of sufferers are more likely to have the condition than the population at large.<ref>{{cite journal | author = Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S | title = Genetics of cluster headache: an update. | journal = J Headache Pain | volume = 6 | issue = 4 | pages = 234-6 | year = 2005 | month = September 2005 | id = PMID 16362673}} </ref> | |||
* There is a [[genetics|genetic]] component to cluster headaches, although no single [[gene]] has been identified as the cause. | |||
* First-degree relatives of sufferers are more likely to have the condition than the population at large.<ref>{{cite journal | author = Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S | title = Genetics of cluster headache: an update. | journal = J Headache Pain | volume = 6 | issue = 4 | pages = 234-6 | year = 2005 | month = September 2005 | id = PMID 16362673}} </ref> | |||
* Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies. | |||
===Triggers=== | ===Triggers=== | ||
| Line 47: | Line 32: | ||
* Napping causes a headache for some sufferers. | * Napping causes a headache for some sufferers. | ||
* The role of diet and specific foods in triggering cluster headaches is controversial and not well understood. | * The role of diet and specific foods in triggering cluster headaches is controversial and not well understood. | ||
=== Associations: === | |||
Cluster headaches may also be associated with or secondary to other conditions such as: | |||
* Hypothalamic and pituitary tumors | |||
* Meningiomas (anywhere from the cavernous sinus to the upper cervical spine) | |||
* Carotid artery dissections | |||
* Vascular malformations | |||
* Sleep apnea | |||
==References== | ==References== | ||
Revision as of 01:38, 26 May 2020
|
Cluster Headache Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Cluster headache pathophysiology On the Web |
|
American Roentgen Ray Society Images of Cluster headache pathophysiology |
|
Risk calculators and risk factors for Cluster headache pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Sabeeh Islam, MBBS[2], Saumya Easaw, M.B.B.S.[3]
Overview
Cluster headaches are classified as vascular headaches. The intense pain is caused by the dilation of blood vessels which creates pressure on the trigeminal nerve. While this process is the immediate cause of the pain, the etiology (underlying cause or causes) is not fully understood.
Pathophysiology
Cluster headaches are classified as vascular headaches. The intense pain is caused by the dilation of blood vessels which creates pressure on the trigeminal nerve. While this process is the immediate cause of the pain, the etiology (underlying cause or causes) is not fully understood.
Hypothalamus
Among the most widely accepted theories is that cluster headaches are due to an abnormality in the hypothalamus; a British specialist of the disease, Dr. Goadsby has developed this theory. This can explain why cluster headaches frequently strike around the same time each day, and during a particular season, since one of the functions the hypothalamus performs is regulation of the biological clock. Metabolic abnormalities have also been reported in patients.
The hypothalamus is responsive to light—daylength and photoperiod; olfactory stimuli, including pheromones; steroids, including sex steroids and corticosteroids; neurally transmitted information arising in particular from the heart, the stomach, and the reproductive system; autonomic inputs; blood-borne stimuli, including leptin, ghrelin, angiotensin, insulin, pituitary hormones, cytokines, blood plasma concentrations of glucose and osmolarity; stress; etc. These particular sensitivities may underlay the causes, triggers, and methods of treatment of cluster headaches.
The above Positron emission tomography pictures indicate the brain areas which are activated during pain only, compared to the pain free periods. These pictures show brain areas which are always active during pain in the yellow/orange color (called "pain matrix"). The area in the center (in all three views) is specifically activated during cluster headache only. The bottom row Voxel-based morphometry (VBM) pictures show structural brain differences between cluster headache patients and people without headaches. Only one area is different: This area is identical with the area of CH specific pain. This area is the hypothalamus.[1][2]
Genetics
- There is a genetic component to cluster headaches, although no single gene has been identified as the cause.
- First-degree relatives of sufferers are more likely to have the condition than the population at large.[3]
- Orexin/hypocretin receptor 2 (HCRTR2) gene mutations are found to be particularly associated with cluster headaches in a couple of separate independent studies.
Triggers
- Nitroglycerin (glyceryl trinitrate) can sometimes induce cluster headaches in sufferers in a manner similar to spontaneous attacks.
- Ingestion of alcohol is recognized as a common trigger of cluster headaches when a person is in cycle or susceptible.
- Exposure to hydrocarbons (petroleum solvents, perfume) is also recognized as a trigger for cluster headaches.
- Some patients have a decreased tolerance to heat, and becoming overheated may act as a trigger.
- Napping causes a headache for some sufferers.
- The role of diet and specific foods in triggering cluster headaches is controversial and not well understood.
Associations:
Cluster headaches may also be associated with or secondary to other conditions such as:
- Hypothalamic and pituitary tumors
- Meningiomas (anywhere from the cavernous sinus to the upper cervical spine)
- Carotid artery dissections
- Vascular malformations
- Sleep apnea
References
- ↑ May et al.: PET and MRA findings in cluster headache and MRA in experimental pain Neurology 2000;55:1328-1335, PMID 11087776.
- ↑ Dasilva AF, Goadsby PJ, Borsook D: Cluster headache: a review of neuroimaging findings. Curr Pain Headache Rep. 2007;11(2):131-6. PMID 17367592.
- ↑ Pinessi L, Rainero I, Rivoiro C, Rubino E, Gallone S (2005). "Genetics of cluster headache: an update". J Headache Pain. 6 (4): 234–6. PMID 16362673. Unknown parameter
|month=ignored (help)